过剩1
葡萄糖转运蛋白
效应器
体内
糖酵解
细胞生物学
葡萄糖摄取
生物
葡萄糖转运蛋白1型
细胞生长
T细胞
碳水化合物代谢
化学
新陈代谢
内分泌学
生物化学
免疫系统
免疫学
胰岛素
生物技术
作者
Andrew N. Macintyre,Valerie A. Gerriets,Amanda Nichols,Ryan D. Michalek,Michael C. Rudolph,Divino Deoliveira,Steven M. Anderson,E. Dale Abel,Benny J. Chen,Laura P. Hale,Jeffrey C. Rathmell
标识
DOI:10.1016/j.cmet.2014.05.004
摘要
CD4 T cell activation leads to proliferation and differentiation into effector (Teff) or regulatory (Treg) cells that mediate or control immunity. While each subset prefers distinct glycolytic or oxidative metabolic programs in vitro, requirements and mechanisms that control T cell glucose uptake and metabolism in vivo are uncertain. Despite expression of multiple glucose transporters, Glut1 deficiency selectively impaired metabolism and function of thymocytes and Teff. Resting T cells were normal until activated, when Glut1 deficiency prevented increased glucose uptake and glycolysis, growth, proliferation, and decreased Teff survival and differentiation. Importantly, Glut1 deficiency decreased Teff expansion and the ability to induce inflammatory disease in vivo. Treg cells, in contrast, were enriched in vivo and appeared functionally unaffected and able to suppress Teff, irrespective of Glut1 expression. These data show a selective in vivo requirement for Glut1 in metabolic reprogramming of CD4 T cell activation and Teff expansion and survival.
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